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princip, pharm, phys, regional > princip.-anaphylax. in anesth. > Flashcards

princip.-anaphylax. in anesth. Flashcards

1
Q

difference between anaphylaxis and anaphylactoid reactions?

A
  1. anaphylaxis-IgE mediated response that releases potent mediators from tissue mast cells and basophils, severe systemic reaction.
  2. anaphylactoid- NON IgE mediated response to allergan which is caused by mediators from tissue mast cells and basophils; some are self limiting
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2
Q

what is the % and time frame of allergic reactions? what is the mortality rate?

A

90% occur within 3 minutes, 3.4% mortality

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3
Q
  1. Specific immune system response consists of:

2. types of specific immunity:

A
  1. response that results from destruction of foreign matter and antigens to protect from injury
  2. inate immunity, acquired immunity, humoral response
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4
Q

non specific immunity consists of:

A
  1. plama proteins/ complement system
  2. acquired immunity (from vaccination)
  3. passive immunity (antibodies and activated T cells- temporary from hours to weeks)
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5
Q
  1. what is the complement system?
  2. how does it work?
  3. what are the principal complement proteins?
  4. what 2 pathways activate the proteins?
A
  1. a system of 20 different plasma proteins
  2. plasma proteins bind to activated antibodies, other complement proteins, cell membranes
  3. C1-C9, B & D which are normally incative
  4. IgE & IgM binding to antigen or alternative path by endotoxin or drug reaction
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6
Q
  1. function of complement system:
  2. what is normal state of compliment system
  3. what regulates it?
A
  1. recognize bacteria directly and indirectly
  2. usually off
  3. regulated by inhibitors
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7
Q
  1. what are antigens also called?
  2. what is an important charecteristic as far as response to antigens?
  3. what are the small substances called, how small are they, and what do they do in order to elicit a response?
A
  1. immunogens
  2. specificity of response
  3. less than 8,000 mw, called haptens, must combine with protein or macromolecule to elicit immune response
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8
Q

examples of haptens:

A
  1. drugs or drug metabolites
  2. chemicals in dust
  3. animal dander
  4. poison ivy
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9
Q

are haptens antigenic by themselves

A

no, only when combined with macromolecules

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10
Q

what is angioneurotic edema?

A

the result of a deficiency of C1 compliment system inhibitor

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11
Q

what are antigens?

A

molecules capable of iliciting an immune response

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12
Q

what are examples of Haptens?

A

drugs and metabolites
chemicals in dust
animal dander
poison ivy

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13
Q

what are antibodies?

A 
protein immunoglobbulin that can recognize and bind to a specific antigen
function as specific receptor molecules located on different immune cell surfaces
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14
Q

what causes activation of antibodies

A

antigen-antibody binding; dependent on cell type

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15
Q

what are the 5 classes of antibodies?

A 
IgG
IgA
IgM
IgD
IgE
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16
Q

name the effector cells and proteins of the nonspecific immune response:

A
  • monocytes and macrophages
  • neutrophils
  • eosinophils
  • basophils
  • mast cells
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17
Q

job of monocytes and macrophages

A
  • involved in processing and presenting antigens to T-cell lymphocytes
  • effect inflammatory, tumoricidal and microbicidal functions
  • predominant cells at sites of chronic inflammation
  • phagocytize and digest invading organisms
  • macrophages arise from circulating monocytes or may be confined to specific organs (lung macrophages, lymp macrophages, spleen macrophages).
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18
Q

neutrophil facts:

A
  • first cell to appear in an acute inflammatory reaction
  • contains substances that aid in microbial killing such as
  • –enzymes
  • –proteases
  • –acids
  • –hydroxyl radicals
  • –hydrogen peroxide
  • –super oxide
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19
Q

eosinophil facts:

A
  • exact function unclear
  • associated with parasitic infections
  • secrete enzymes that limit response of other inflammatory cells (histhamine)
  • other cells (mast cells, basophils) secrete eosinophilic chemotactic factor that recruits eosinophils to accumulate at sites of infection, tumors and allergic reactions (remember allergic asthma from physio).
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20
Q

basophil facts:

A
  • compise less than 0.5 to 1% of circulating granulocytes
  • have IgE mediators that are released when activated
  • similar in function to mast cells, but have capacity for chemotactic migration in response to other stimulus
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21
Q

mast cells:

A
  • important mediator in immediate hypersensitivity reactions
  • located on the tissue of perivascular spaces of skin, lungs, intestines
  • on the surface of IgE receptors that bind to specific antigens; once activated, these cells release physiologically active mediators important to immediate hypersensitivity responses such as histhamine, heparin and proteases
  • CENTRAL STEP in anaphylactic syndrome is the activation of mast cells and basophils
  • mediators released form mast cells and basophils carse severe and abrupt physiologic alterations
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22
Q

hypersensitity responses; name the types

A

type I thru type IV

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23
Q
  1. what is a type I hypersensitive response:

2. what are examples?

A
  1. immediate hypersensitivity reaction caused by antigens binding to IgE on surface of mast cells; triggers release of intracellular granules
  2. anaphylaxis, extrensic asthma, allergic rhinitis
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24
Q
  1. what is a Type II hypersensitive reaction:

2. give examples:

A
  1. cytotoxic hypersensitivity reaction caused by antigen (foreign protein) binding with IgG or IgM, causing cytolysis and phagocytosis.
  2. hemolytic reaction
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25
Q
  1. type III hypersensitive response:

2. examples:

A
  1. imune complex disease caused by internal or external antigens binding with IgG, IgM, or IgA, which results in inflammatory reaction.
  2. snake venom reaction, systemic lupus, post strep nephritis
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26
Q
  1. type IV hypersensitive reaction
  2. what is different with this type of reaction?
  3. examples:
A
  1. delayed response involving sensitized T lymphocytes to specific antigens.
  2. does not require antibodies for reaction
  3. contact dermatitis, tissue/ organ rejection
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27
Q

what immunoglobulin binding to an antigen initiates anapylactic reactions?

A

IgE

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28
Q

what is important about anaphylactic reactions in terms of sensitization?

A

you must come in contact with that antigen substance or one similar to produce sentization.

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29
Q

what happens on re-exposure to the antigen or substance?

A
  1. the antigen is bound and bridges two immunospecific IgE antibodies located on the surface of mast cells and basophils
  2. this causes the release of histhamine and chemotactic factor of anaphylaxis
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30
Q

what are the chemical mediators of anaphylaxis?

A
  1. histhamine
  2. chemotactic factor of anaphylaxis
  3. leukotrienes
  4. prostaglandins (D2 & PGE)
  5. Kinins
  6. platelet activating factor (PAF)
  7. tryptase
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31
Q

histhamine facts:

  1. what does it stimulate?
  2. what does it cause in vessels?
  3. what does it cause in cardiovascular system
  4. coronary artery effects
  5. how is it broken down (where)
A
  1. H1&H2 receptors
  2. vasodilates vessels and increases capillary permeability
  3. causes tachycardia and decreased SVR (hypotension)
  4. causes coronary vasoconstriction
  5. rapidly metabolized by endothelial enzymes
32
Q

facts about chemotactic factors of anaphylaxis:

  1. released from what cells?
  2. cause ___ migration (this migration is called_____)
  3. role in ____ _____ ____ is unclear?
  4. activation of (answer #2.a) may be responsible for what?
A
  1. mast cells and basophils
  2. granulocyte migration; chemotaxis
  3. acute allergic response
  4. granulocytes; recurrent manifestations of anaphylaxis
33
Q

leukotrienes:

  1. how fast do they react in anaphylaxis?
  2. is a product of breakdown of what?
  3. what does it cause (resp, vessels (2 things), cardiac?
A
  1. slow reacting
  2. arachidonic acid breakdown
  3. produces
    - bronchoconstriction
    - increased capillary permeability
    - vasodilation
    - myocardial depression
34
Q

prostaglandins

  1. what do they produce?
  2. what do they mediate; are they powerful?
  3. cause: (vessel (2 things), respiratory, cardiopulmonary)
A
  1. product of arachadonic acid metabolism by the (COX) cyclo-oxygenase patheway
  2. mast cell mediator; yes,potent
  3. cause:
    - vasodilation
    - increased capillary permeability
    - bronchospasm
    - pumonary HTN
35
Q
  1. what is prostaglandin D2?

2. what does it cause?

A
  1. major metabolite of mast cells

2. vasodilation and bronchospasm

36
Q

what is prostaglandin PGE2

A

a potent bronchoconstrictor

37
Q
  1. what is a kinin

2. what does it cause vascular (2), and pulmonary

A
  1. a small peptide synthesized in the mast cells and basophils
  2. causes vasodilation, increased capillary permeability and bronchospasm
38
Q
  1. what is platelet activating factor?

2. what effects does it cause in heart (2), pulmonary, pulmonary-vascularly?

A
  1. potent material producing aggregation of platelets and probably leukocytes for inflammation products
    • decreased myocardial contraction force
    • coronary vasoconstriction
    • increased PVR (pulm.vasc. resist.)
    • pulmonary edema
39
Q
  1. what is tryptase?
  2. what are effects?
  3. how long does it last; why is that important?
A
  1. tryptase is a chemical released by histhamine
  2. increases vascular permeability and may be the cause of airway edema
  3. longer half live (lasts hours); may be a good marker of histhamine liberation.
40
Q

name some IgE mediated reactions:

A
  1. foods
  2. venoms
  3. vaccines
  4. allergy extracts
  5. latex
41
Q

complement activation reactions (C3a, C5a)

A
  1. blood products

2. immunoglobulins

42
Q

direct activation reactions:

A
  1. contrast dye
  2. opiates
  3. dextran
  4. ??exercise
43
Q

cyclo-oxygenase inhibitors;

A
  1. nsaids, asa

2. tartrazine

44
Q

what can eosinophils do that you won’t see?

A

cause late phase reactions

45
Q

what are signs and symptoms of anaphylaxis?

A
  1. impending sense of doom, lightheadedness
  2. CV signs (predominate during anesthesia)
  3. shock
  4. laryngeal edema
  5. bronchospasm (s/s wheezing, dib)
  6. urticaria (hives) or flushing
  7. angioedema (lips, tongue)
    8.GI symptoms
    9 rhinitis
46
Q

Non IgE-mediated reactions:

  1. how is it different from IgE mediated?
  2. what are the symptoms?
  3. what are usual suspects
A
  1. only histhamine is released (no other mediators)
  2. same as IgE
  3. opiates, NDMRs
47
Q

what is the onset of anaphylaxis?

A

2-20 min

48
Q

what cv signs might you see with anaphylaxis?

A

dysrhythmias, palpitations, tachycardia, ekg changes, pac/pvcs, hypotension, shock, ischemia, circulatory collapse

49
Q

what hematological signs might you see with anaphylaxis?

A

fibrinolysis, DIC

50
Q

what neuro symptoms

A

headache, confusion, anxiety, seizures, coma

51
Q

gi symptoms

A

N/V, dysphagia, cramping, increased mucous, diarrhea

52
Q

GU

A

pelvic pain, incontinence

53
Q

cutaneous/integumentary

A

urticaria, pruritis, angioedema

54
Q

eyes

A

itching, tearing, conjunctivitis

55
Q

what other conditions might anaphylaxis mimic?

A

MI, PE, irritant induced bronchospasm, aspiration

56
Q

best prevention of anaphylaxis?

A
  1. prevention
  2. good medical history taken
  3. diagnstics (skin testing, radioallergosorbent test (RAST), ELISA (enzyme linked immunosorbent assay)
  4. monitor and take precautions for risk groups (multiple surgeries, multiple allergies etc.)
57
Q

treatment of anaphylaxis

A
  1. recognize early
  2. maintain CV/resp (mortality primarily associated with compromise of these).
  3. stop administration of offending agent
  4. discontinue anesthetic agents
  5. consider SQ or aerosolized epi for laryngeal edema
  6. intubation or cric (if necessary)
  7. FLUIDS (rapidly)–20-50 ml/kg for hypotension
58
Q

doses of epi for anaphylaxis: (all titrated to effect of course!!!)

A
  1. 0.01-0.03 ml/kg increments of 1:1000 SQ
  2. 1-3 ml of 1:10,000 epi (o.1 mg/ml over 10 minutes
  3. 1-4 mcg/min of 1 ml of 1:1,000 epi in 250 m (i.e. 0.25-1.0 ml/min of a 4mcg/ml concentration).
  4. 10 mo of 1:10,000 via ETT
59
Q

secondary therapy:

A
  1. benadryl 1mg/kg iv or im (50 mg max)
  2. rantidine 1mg/kg iv (50 mg max)
  3. Glucocorticoid: hydrocortisone (0.25 to 1 g) or solumedrol 30-35 mg/kg
  4. aminophylline (5-6 mg/kg loading dose) followed by infusion of 0.5-1mg/kg/hr (check blood level at some point)
  5. inhaled beta 2 agonists
  6. epi 0.02-0.05 mcg/kg/min (2-4 mcg/min) or Norepi 0.05 mcg/kg/min (2-4 mcg/min) or dopamine 5-20 mgc/kg/min
  7. bicarb 0.5-1mg/kg, titrate to ABGs
60
Q

muscle relaxant reactions:

  1. how often does this happen in peri-op?
  2. what % of patients allergic to one will be allergic to the next?
  3. why are there so many cross sensitivities with MRs?
  4. why is anaphylactic response high with MRs?
  5. what other factors/ products may explain the high rate of reactions?
  6. who makes up the majority of these reactions, why?
A
  1. make up majority of reactions in perioperative period
  2. 50%
  3. many MRs have similar chemical makeup (especially quarternary ammoniums)
  4. IgE reacts especially quartenary and tertiary ammonium ions
  5. cross sensitivity with other compounds (food, cosmetics, disinfectants, industrial materials)
  6. 90-95% female (possibly due to ion epitopes in cosmetics).
61
Q

induction agent allergic reactions:

  1. how often does a barbiturate reaction occur?
  2. barb reactions usually occur in persons with allergies to ___? what symptoms might they experience
  3. how small of a dose of thiopental can cause a reaction in highly sensitized persons?
  4. what induction agent has caused severe anaphylaxis?
  5. what chemical structures are persons allergic to porpofol, MRs, LAs, and abx reacting to?
  6. propofol allergy usually coincides with allergy to ___?
  7. etomidate allergy different cause it usually manifests where?
A
  1. 1 out of 30,000
  2. allergies to food; asthma and rhinitis
  3. 10 ug of thiopental
  4. propofol
  5. phenyl nucleus and isopropyl side chain
  6. eggs
  7. GI and cutaneous
62
Q

Local anesthetic allergy:

  1. how often and why are they probably missed?
  2. if allergic to one, will you be allergic to another?
  3. IgE reactions usually with what preservative metabolite?
A
  1. rare and often confused with vasovagal changes, accidental venous injection, the epi mixed with the LA, or psychomotor responses
  2. usually among the classes but no cross class sensitivity
  3. mostly to parabens (esters)
63
Q

opiate reactions:

  1. how often?
  2. what drugs are usual suspects?
  3. what are symptoms?
  4. how ling do they last?
A
  1. rare since opiates mimic natural endorphins
  2. morphine and demorol (non immunological histhamine release)
  3. skin issues (hives, itching etc.), mild hypotension, anaphylaxis is rare
  4. self limiting
64
Q

pcn reactions:

  1. how common compare to all abx? what %
  2. how often are they anaphylactic
  3. fatality rate %, annual numbers
  4. how does pcn cause a reaction?
  5. in whom do most of the serious and fatal pcn reactions occur?
A
  1. most common, 0.7-8%
  2. .004-.015%
  3. 1 out of 50-100,000; 400-800 deaths annually
  4. pcn binds with haptens (macro-proteins) before it can cause reaction
  5. persons with known PCN allergy
65
Q

cephalosporin reactions:

  1. what cross sensitivity is common to cephalosporin reaction?
  2. what is the mechanism of allergy to ceph’s?
  3. what test would preclude a patient form taking ceph’s?
A
  1. PCN allergy
  2. unkonwn
    • skin test to PCN
66
Q

beta lactam abx:

what other abx have cross sens. with PCN

A

carbapenems (imipenem) and monobactans (aztreonam)

67
Q

vancomycin:

  1. what kind of reactions happen with vanco (on cellular level)?
  2. what are common reactions seen?
  3. what is one of the lowest adult doses and what is the fastest it can run?
A
  1. non immunologically mediated histhamine release
  2. hypotension and red man syndrome when given too fast
  3. 500 mg/100 ml over 60 minutes
68
Q

sulfa drug reactions:

  1. what are common symptoms and at what time interval do they occur?
  2. who is most likely to have a sulfa reaction?
  3. what immunoglobulin will react to sulfa?
  4. what must happen to sulfa in the body before it will react?
A
  1. skin eruptions and drug fever betwen days 7-10 of treatment
  2. 10-15 x higher in patients with AIDS
  3. IgE ab
  4. must be metabolized by liver into metabolite that is immunogenic (causes reactions)
69
Q

X-ray dye (radiocontrast media):

  1. how often is there a reaction?
  2. how often are they fatal?
  3. most reactions occur within what time frame?
  4. persons with previous reaction are how likely (%) to react again?
  5. is it IgE mediated?
  6. what response pathway is responsible, what is released, what cells are activated?
  7. there IS histhamine release, but where does it come from?
A
  1. 5-8% (2-3% are anaphylactoid)
  2. 1 of 50,000 fatal
  3. first 3-5 minutes
  4. 33% chance
  5. no
  6. complement system either via classic or alternate pathway causes production of anaphylactotoxins with mast cell and basophil release
  7. histhamine can be released from mast cells and basophils separate from complement system d/t hypertonicity of dye
70
Q

protamine allergy:

  1. what are s/s
  2. what patient population is at risk #1
  3. what other patients have high chance of reacting
  4. what obvious patients will react (hint: made from salmon testis)
A
  1. rash, urticaria, bronchospasm, hypotension
  2. diabetics receiving insulin containing protamine have 30-50x higher risk of deadly reactions when given IV protamine
  3. vasectomy patients have 20-33% chance of having antibodies
  4. patients with fish allergies
71
Q

latex allergy;

  1. incidence?
  2. what pediatric patient has very high risk?
  3. what adults group (that you know) has high risk?
  4. what other patients have high risk?
  5. what are symptoms
  6. what symptom has a delayed onset and what does it look like?
  7. what about a each subsequent exposure?
  8. what tissue areas really react severely?
  9. what is a cause of respiratory reactions that we must watch out for?
  10. is there a immunization or desentization regimen for latex?
  11. how is latex allergy diagnosed?
  12. whats the best way to minimize latex allergies
  13. who in the OR should be wearing latex free gloves if patient has allergy?
A
  1. 1-6% of population
  2. spina bifida as high as 73% chance
  3. health care workers 8-20% chance
  4. patients having multiple surgeries, chronic bladder caths, atopic individuals, fruit allergies
  5. contact urticaria to anaphylaxis with laryngeal edema
  6. can be delayed and looks like poison ivy
  7. each subsequent reaction takes less and is more severe with potential chronic effects
  8. contact with mucous membranes (including dental, rectal, vaginal)
  9. aerosolized latex
  10. no
  11. diagnosed by history, labs, skin test, RAST
  12. avoid and symptomatic treatment
  13. EVERYONE!!!
72
Q

management of latex allergy:

  1. how do you keep cross contamination of latex from affecting allergic patients?
  2. what are other things that can be done?
A
  1. make them the first case of day
  2. –
    - minimize pre op exposure
    - remove all latex from or
    - use only latex free ports
    - remove stoppers from multidose vials
    - everyone (all caregivers) should know about allergy
73
Q

latex allergy in the or:

  1. when do symptoms usually occur
  2. symptoms in awake patient?
A 
1. within 30 min of exposure
can occur from 10-290 minutes later
2. 
-itchy eyes
-prurutis
-SOB
-wheezing
-hoarseness
-laryngeal edema
-faintness
-impending doom
-restlessness
-agitation
-n/v
-abdominal cramping and diarrhea
74
Q

latex allergy in anesthetized patient:

s/s:

A
  • tachy
  • hypotensive
  • wheezing
  • bronchospasm
  • cardio/pulmonary arrest
  • flushing
  • facial edema
  • laryngeal edema
  • urticaria
75
Q

treatment for latex allergy in anesthetized patients:

A
  1. treat allergy symptoms
  2. ABCs
  3. 100% oxygen
    (pre treatment if good for known allergy patients)
76
Q

1 cause of anaphylaxis

A

Ndmr-ammoniums (roc etc).

princip, pharm, phys, regional (18 decks)

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